Tardive dyskinesia (TD), a disorder of involuntary movements, is arguably one of the most serious iatrogenic effects of the neuroleptic treatment of schizophrenia. Although the pathophysiology and anatomical substrate of TD has not been established, research has implicated the basal ganglia as one of the primary sites of dysfunction. Many researchers have attempted to identify clinical and neurobiological variables that are either associated with the disorder or that are risk factors for its development. For instance, most available studies show that schizophrenics with TD demonstrate more severe cognitive deficits than schizophrenic patients without TD. Although impairments have been demonstrated on a variety of tasks, the majority of studies have indicated differences in tasks requiring learning and memory. One away to further investigate the- neuropsychological profile of persons with TD is to arrow from literature examining other basal ganglia disorders. A number of studies have shown that patients with basal ganglia dysfunction demonstrate specific impairments in procedural learning and memory. The overall goal of the proposed project is to examine the integrity of both procedural and declarative memory systems in schizophrenic patients with TD. Although several investigators have suggested that patients with TD exhibit impairments in the declarative memory system; no study has investigated TD patients' performance on tasks requiring procedural learning and memory. - One hundred twenty subjects will be evaluated on tests of declarative and procedural learning and memory. Procedural tests include one traditional measure (rotor pursuit) and two new measures (prism adaptation and reaction time tracking). Declarative tests include standardized tests of clinical neuropsychology. This investigation is particularly important given the implications of the basal ganglia in procedural knowledge. Improved understanding of learning and memory deficits in TD may lead to (a) more precise characterization of different types of procedural and declarative memory systems in patients with basal ganglia dysfunction; (b) better understanding of the potential effects of neuroleptic exposure to dissociable memory systems; (c) future development of more sensitive clinical tests for early detection of procedural. deficits in patients with basal ganglia dysfunction; (d) better understanding of brain mechanisms related to tardive dyskinesia.